Implantable medical electrical stimulation and/or sensing leads (electrical medical leads) are well known in the fields of tissue stimulation and monitoring, including cardiac pacing and cardioversion/defibrillation, and in other fields of electrical stimulation or monitoring of electrical signals or other physiologic parameters. In the field of cardiac stimulation and monitoring, the electrodes of epicardial or endocardial cardiac leads are affixed against the epicardium or endocardium, respectively, or inserted therethrough into the underlying myocardium of the heart wall.
Epicardial or myocardial cardiac leads, or simply epicardial leads, are implanted by exposure of the epicardium of the heart typically through a limited thorocotomy or a more extensive surgical exposure made to perform other corrective procedures. Endocardial cardiac leads, or simply endocardial leads, are implanted through a transvenous route to locate one or more sensing and/or stimulation electrode along or at the distal end of the lead in a desired implantation site in a chamber of the heart or a blood vessel of the heart. It is necessary to accurately position the electrode surface against the endocardium or within the myocardium or coronary vessel at the implantation site.
A passive or active fixation mechanism is typically incorporated into the distal end of permanent cardiac leads and is deployed at the implantation site to maintain the distal end electrode in contact with the endocardium or within the myocardium. Considerable effort has been undertaken to develop passive and active fixation mechanisms that are simple to use and are reliable in maintaining the distal electrodes in position.
Active fixation mechanisms are designed to penetrate the epicardial or endocardial surface and lodge in the myocardium without perforating all the way through the myocardium. The most widely used active fixation mechanism employs a helix, which typically also constitutes a pace/sense electrode. Typically, a mechanism is used to shield the sharpened tip of the helix during the transvenous advancement into the desired heart chamber or coronary vessel or to the epicardial surface. In one approach, a retraction mechanism that retracts the helix into a distal cavity of the lead body as shown in U.S. Pat. Nos. 5,837,006 and 6,298,272, for example, is employed. In another approach, a shroud, e.g., a plug of dissolvable biocompatible material as disclosed in U.S. Pat. No. 5,531,783, for example, is applied over and between the coil turns of the helix. In still another approach, the lead is introduced through the sheath of a guide catheter, as disclosed in U.S. Pat. No. 6,408,214, for example, that is advanced to the implantation site. The helix is advanced from the sheath or out of the lead body or the plug dissolves when the desired implantation site is reached. In one manner or another, the helix is adapted to be rotated by some means from the proximal end of the lead body outside the patient's body in order to screw the turns of the helix into the myocardium and permanently fix the pace/sense electrode.
Over the last 30 years, it has become possible to reduce endocardial lead body diameters from 10 to 12 French (3.3 to 4.0 mm) down to 2 French (0.66 mm) presently through a variety of improvements in conductor and insulator materials and manufacturing techniques. The lead bodies of such small diameter, 2 French, endocardial leads are formed without a lumen that accommodates use of a stiffening stylet to assist in implantation.
Such a small diameter endocardial lead is formed with an active fixation helix that extends distally and axially in alignment with the lead body to a sharpened distal tip and that has a helix diameter substantially equal to the lead body diameter. The fixation helix does not necessarily increase the overall diameter of the endocardial lead, and fixation is relatively robust once the helix is screwed into the myocardium. Typically, but not necessarily, the fixation helix is electrically connected to a lead conductor and functions as a pace/sense electrode. In some cases, the lead body encloses one or more helical coiled or stranded wire conductor and lacks a lumen.
When the fixation helix is used as a pace/sense electrode, the surface area of the fixation helix must be controlled within a range that historically has been between 6-10 mm2, typically 8 mm2. The fixation helix outer diameter approximates the lead body diameter, and the fixation helix typically has more than one coil turn. More recent, small diameter fixation helices have surface areas in the range of 2.0 mm2 to 5.0 mm2 typically 4.0 mm2. The number of turns and length of the fixation helix is selected to avoid perforation through the heart wall. The exposed electrode surface must be within the myocardium rather than exposed outside the heart or inside a heart chamber.
Consequently, it is conventional to coat a part or parts of the fixation helix with electrical insulation to control the exposed surface area and to ensure that the exposed portion of the helix remains within the myocardium when the helix is properly screwed in. See, for example, U.S. Pat. Nos. 4,000,745, 4,010,758, 5,143,090, and 6,501,994 and U.S. Patent Application Publication Nos. 2003/0060868 and 2003/0163184. Electrically insulating coatings are also applied to portions of barbed electrodes of epicardial leads as shown, for example in commonly assigned U.S. Pat. No. 4,313,448. Electrical insulation of a fixation helix that is not employed as a pace/sense electrode is shown, for example, in U.S. Pat. No. 4,662,382. Various forms of selective electrical insulation of other shapes of pace/sense electrodes are shown in U.S. Pat. Nos. 4,026,303 and 6,526,321 and in EP Publication No. 0 042 551.
The dielectric, biocompatible, insulating coatings of choice have included silicone rubber and non-thrombogenic compounds such as Parylene C™ parylene, and various polyurethanes, polyacrylates (including polymethacrylates), polyesters, polyamides, polyethers, polysiloxanes, polyepoxide resins and the like. Cross-linked polymers within these classes may be preferred for their resistance to breakdown and their physical durability. Parylene coatings on the surfaces of implantable medical devices have been widely accepted, and the deposition of a parylene coating on a pace/sense electrode can be readily effected using a parylene vacuum deposition system that delivers poly-paraxylylene into a vacuum chamber containing the targeted electrode. The portions of the deposited parylene coating can be etched away as disclosed in the above-referenced '321 patent to expose the pace/sense electrode surface.
The ideal electrode impedance for chronic pacing across the electrode-tissue interface is in the range of 800 to 1,000 ohms. For example, the impedances reported in the above-referenced '994 patent are about 800 ohms measured during chronic implantation. The perforation of the myocardium by the fixation helix causes inflammation and cell death, particularly of myocardial cells between the turns of the helix and within the helix lumen, and impedance rises for a time following implantation to about 1200 ohms, for example, before falling to the chronic impedance level. Cell death and substitution of scar tissue for excitable myocardial cells is responsible for the observed impedance changes. Steroid eluting coatings and devices are commonly incorporated into the distal end of the lead body to counter post-implantation impedance rise as described in the above-referenced '994 patent and in U.S. Pat. No. 5,324,325, for example.
Pace/sense electrodes are typically formed of platinum or platinum iridium alloys that are bio-compatible and bio-stable during chronic implantation and delivery of pacing pulses. Consequently, fixation helices used as pace/sense electrodes are formed of platinum or platinum iridium wire wound into the helical shape to have one or more coil turn terminating in a sharpened tip. It is also common practice to surface treat or etch the electrode surface area of helical screw-in electrodes or to coat the electrode surface area with platinum black or a platinum metal oxide to create a surface texture that enhances the characteristics of the tissue-electrode interface to decrease post pulse delivery polarization and stabilizes impedance changes, as disclosed in U.S. Pat. No. 4,762,136, for example.
It is not convenient to surface treat the fixation helix, coat the surface treated helix with a dielectric insulating layer, and then selectively etch away the insulating layer to expose the pace/sense electrode surface as suggested in the above-referenced '321 patent, since the etching may damage an electrode coating or surface treatment.
Moreover, the selective insulation techniques and resulting electrode surface areas on pace/sense screw-in electrodes disclosed in the prior art fail to address the injury and cell death occurring within the lumen of the fixation helix.